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Decreased Axon Flare Reaction to Electrical Stimulation in Patients With Chronic Demyelinating Inflammatory Polyneuropathy

Kokotis, Panagiotis; Schmelz, Martin; Papagianni, Aikaterini E.; Zambelis, Thomas; Karandreas, Nikos

Journal of Clinical Neurophysiology: March 2017 - Volume 34 - Issue 2 - p 101–106
doi: 10.1097/WNP.0000000000000294
Original Research

Purpose: In chronic inflammatory demyelinating polyradiculopathy (CIDP), the impairment of unmyelinated nerve fibers appears unexpected. The measurement of the electrically induced axon flare reflex is a clinical test to assess the peripheral C-nociceptor function. In this study, we compared the flare area in patients suffering from CIDP with healthy subjects.

Methods: We examined 18 patients fulfilling the criteria for CIDP (11 men, mean age 51.8 years, SD 15.1) and 18 age-matched adult healthy volunteers (control group) (11 men, mean age 51.9 years, SD 15.8). The flare responses were elicited by transcutaneous electrical stimulation and recorded by laser Doppler imaging.

Results: There was a significant reduction of electrically induced maximum flare area in the foot dorsum of patients with CIDP (t-value 2.08, P = 0.04) which proved to be length-dependent measured by a numerical index comparing the results with the forearm and thigh. The repeatedmeasures ANOVA revealed statistically significant smaller flare areas in all body regions for the CIDP group (P < 0.001).

Conclusions: The axon flare reaction to electrical stimulation was decreased in patients with chronic demyelinating inflammatory polyneuropathy. The evaluation of the axon flare response can be proposed as a noninvasive objective functional test to detect an impaired C-fiber function in CIDP patients with the advantages of simplicity of the procedure, time economy, and objectivity.

*Laboratory of Electromyography and Clinical Neurophysiology, Department of Neurology, Aeginition Hospital, University of Athens, Athens, Greece;

Department of Anesthesiology and Intensive Care Medicine, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany; and

Department of Neurology, University Clinic of Würzburg, Würzburg, Germany.

Address correspondence and reprint requests to Aikaterini E. Papagianni, MD, University Clinik of Wuerzburg, Wuerzburg, Germany; e-mail: Papagianni_A@ukw.de.

The authors declare no conflicts of interest.

Supported in part by the special account for research grants of the National and Capodistrian University of Athens, Greece.

© 2017 by the American Clinical Neurophysiology Society